“…A major and still widely debated topic is whether OBI may contribute to liver damage favoring the progression towards cirrhosis and the development of HCC in patients with CLD caused by different etiologic factors, such as HCV, non-alcoholic fatty liver, and alcohol-use disorders [ 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 ] ( Table 1 ). Indeed, patients who recover from a self-limited HBV acute hepatitis may persistently carry HBV genomes for several decades without showing any clinical or biochemical sign of liver injury [ 122 ], but when their liver tissues are examined, the histological signs of mild hepatic inflammation are revealed [ 123 , 124 ].…”